Aaron Gitler earned his B.Sc. in biochemistry and molecular biology from The Pennsylvania State University. He earned his Ph.D. in cell and molecular biology at the University of Pennsylvania, where he studied endothelial cell signaling pathways in cardiovascular development with Jonathan Epstein. He performed postdoctoral research at the Whitehead Institute for Biomedical Research and the Massachusetts Institute of Technology with Susan Lindquist until 2007, when he joined the faculty of the University of Pennsylvania in the Department of Cell and Developmental Biology. In 2012 he moved to the Stanford University School of Medicine.
Gitler’s research goal is to discover the cellular and molecular mechanisms by which protein aggregates contribute to neurodegeneration, and to harness these mechanisms to devise novel therapeutic strategies. His laboratory uses the baker’s yeast Saccharomyces cerevisiae as a simple, yet powerful, model system to study the cell biology underpinning protein-misfolding diseases, which include Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis (ALS). They have recently focused on the ALS disease proteins TDP-43, FUS/TLS and C9orf72, and have generated yeast models to define mechanisms by which these proteins contribute to ALS. They have used these yeast models to perform high-throughput, genome-wide modifier screens to discover suppressors and enhancers of toxicity. Launching from the studies in yeast, they have extended findings into animal models, and even into human patients. For example, Gitler and his collaborators discovered mutations in one of the human homologs of a hit from the yeast TDP-43 modifier screen, ataxin 2, in ALS patients, as a relatively common genetic risk factor for ALS. In recent work, they have pursued translational approaches to test whether some of the modifier genes from the yeast screens could be therapeutic targets for ALS and related diseases.
